2023
IL‐27 produced during acute malaria infection regulates Plasmodium‐specific memory CD4+ T cells
Macalinao M, Inoue S, Tsogtsaikhan S, Matsumoto H, Bayarsaikhan G, Jian J, Kimura K, Yasumizu Y, Inoue T, Yoshida H, Hafalla J, Kimura D, Yui K. IL‐27 produced during acute malaria infection regulates Plasmodium‐specific memory CD4+ T cells. EMBO Molecular Medicine 2023, 15: emmm202317713. PMID: 37855243, PMCID: PMC10701605, DOI: 10.15252/emmm.202317713.Peer-Reviewed Original ResearchConceptsCD4<sup>+</sup> T cellsT cellsIL-27Malaria infectionCD4<sup>+</sup> T cell responsesCD4<sup>+</sup> T cell subsetsMemory CD4+ T cellsImmune responseCD4+ T cellsNeutralization of IL-27T cell responsesT cell subsetsPathogenic immune responsesHumoral immune responseSingle-cell RNA-seq analysisPlasmodium chabaudiDevelopment of vaccinesAcute infectionCytokine productionEffector responsesChronic phaseActive infectionProliferative capacityAcute phaseInfection
2021
IL-27 signalling promotes adipocyte thermogenesis and energy expenditure
Wang Q, Li D, Cao G, Shi Q, Zhu J, Zhang M, Cheng H, Wen Q, Xu H, Zhu L, Zhang H, Perry RJ, Spadaro O, Yang Y, He S, Chen Y, Wang B, Li G, Liu Z, Yang C, Wu X, Zhou L, Zhou Q, Ju Z, Lu H, Xin Y, Yang X, Wang C, Liu Y, Shulman GI, Dixit VD, Lu L, Yang H, Flavell RA, Yin Z. IL-27 signalling promotes adipocyte thermogenesis and energy expenditure. Nature 2021, 600: 314-318. PMID: 34819664, DOI: 10.1038/s41586-021-04127-5.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAnimalsBariatric SurgeryDisease Models, AnimalEnergy MetabolismFemaleHumansInsulin ResistanceInterleukin-27MaleMiceObesityp38 Mitogen-Activated Protein KinasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReceptors, InterleukinSignal TransductionThermogenesisUncoupling Protein 1ConceptsIL-27Beige adipose tissueAdipose tissueSerum IL-27Diet-induced obesityBariatric surgeryMetabolic morbidityImmunological factorsInsulin resistanceObesity showTherapeutic administrationMetabolic disordersMouse modelObesityPromising targetEnergy expenditureSignaling promotesThermogenesisBody temperatureMetabolic programsImportant roleTissueCritical roleImmunotherapyMorbidity
2020
Loss of IL-27Rα Results in Enhanced Tubulointerstitial Fibrosis Associated with Elevated Th17 Responses.
Coppock GM, Aronson LR, Park J, Qiu C, Park J, DeLong JH, Radaelli E, Suszták K, Hunter CA. Loss of IL-27Rα Results in Enhanced Tubulointerstitial Fibrosis Associated with Elevated Th17 Responses. The Journal Of Immunology 2020, 205: 377-386. PMID: 32522836, PMCID: PMC7368461, DOI: 10.4049/jimmunol.1901463.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseUnilateral ureteral obstructionIL-17AIL-27RαIL-27Ureteral obstructionKidney diseaseIL-27 actsImmune cell infiltratesCytokine IL-27Day of surgeryImmune-mediated pathologyTubular epithelial cellsDegree of injuryFibrosis AssociatedKidney injuryTh17 cellsTh17 responsesCell infiltrateSerum levelsInflammatory cascadeRenal fibrosisIL-17RAImmune cellsChemokine mRNA
2019
Impact of Interleukin-27p28 on T and B Cell Responses during Toxoplasmosis
Park J, DeLong JH, Knox JJ, Konradt C, Wojno EDT, Hunter CA. Impact of Interleukin-27p28 on T and B Cell Responses during Toxoplasmosis. Infection And Immunity 2019, 87: 10.1128/iai.00455-19. PMID: 31548322, PMCID: PMC6867838, DOI: 10.1128/iai.00455-19.Peer-Reviewed Original ResearchConceptsIL-27p28IL-27Parasite-specific antibody titersEffector T cell populationsT cell-mediated pathologyCell-mediated pathologyT cell activityReduced parasite burdenT cell populationsB cell responsesCentral nervous systemInterleukin-27Antibody titersMajor inhibitory effectHeterodimeric cytokineParasite replicationImmune serumNervous systemParasite burdenCell responsesCell activityInhibitory effectIntracellular parasitesCell populationsToxoplasmosisIL-27 and TCR Stimulation Promote T Cell Expression of Multiple Inhibitory Receptors
DeLong JH, O'Hara Hall A, Rausch M, Moodley D, Perry J, Park J, Phan AT, Beiting DP, Kedl RM, Hill JA, Hunter CA. IL-27 and TCR Stimulation Promote T Cell Expression of Multiple Inhibitory Receptors. ImmunoHorizons 2019, 3: 13-25. PMID: 31356173, PMCID: PMC6994206, DOI: 10.4049/immunohorizons.1800083.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB7-H1 AntigenCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCostimulatory and Inhibitory T-Cell ReceptorsCTLA-4 AntigenFemaleInterleukinsLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, Antigen, T-CellReceptors, ImmunologicSpleenToxoplasmaToxoplasmosisTranscriptomeTransfectionConceptsT cell expressionMultiple inhibitory receptorsIL-27Inhibitory receptorsPD-L1LAG-3Cell expressionCTLA-4Effector cell expressionTCR stimulationEffector T cellsIL-27 productionT cell activationTim-3Cell surface moleculesCell-extrinsic factorsT cellsIR expressionCell activationTIGITInfectionTCR signalsSurface moleculesSynergistic inductionVivo overexpression
2018
Cytokine- and TCR-Mediated Regulation of T Cell Expression of Ly6C and Sca-1.
DeLong JH, Hall AO, Konradt C, Coppock GM, Park J, Harms Pritchard G, Hunter CA. Cytokine- and TCR-Mediated Regulation of T Cell Expression of Ly6C and Sca-1. The Journal Of Immunology 2018, 200: 1761-1770. PMID: 29358280, PMCID: PMC5821564, DOI: 10.4049/jimmunol.1701154.Peer-Reviewed Original ResearchConceptsT cell expressionIL-27T cellsEffector cellsSca-1Cell expressionPathogen-specific T cellsMemory precursor effector cellsEndogenous IL-27Identification of CD8Type I IFNMemory stem cellsCytokine-mediated signalsEffector CD4Ly6C expressionSca-1 expressionImmune populationsT-betExpression of Ly6CMemory populationMouse CD4I IFNLy6CIFNMouse splenocytes
2017
Microbiota control immune regulation in humanized mice
Gülden E, Vudattu NK, Deng S, Preston-Hurlburt P, Mamula M, Reed JC, Mohandas S, Herold BC, Torres R, Vieira SM, Lim B, Herazo-Maya JD, Kriegel M, Goodman AL, Cotsapas C, Herold KC. Microbiota control immune regulation in humanized mice. JCI Insight 2017, 2: e91709. PMID: 29093268, PMCID: PMC5752290, DOI: 10.1172/jci.insight.91709.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsAntibodies, AntinuclearAntibodies, Monoclonal, HumanizedAutoimmune DiseasesB7-2 AntigenCD11b AntigenCD11c AntigenCD3 ComplexCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalGastrointestinal MicrobiomeGastrointestinal TractGraft RejectionHumansImmunosuppressive AgentsImmunotherapyInterferon-gammaInterleukin-10Interleukin-27Leukocytes, MononuclearMiceMice, KnockoutMucous MembraneSkin TransplantationSTAT5 Transcription FactorT-LymphocytesTransplantation, HeterologousConceptsT cellsIL-10Humanized miceHuman peripheral blood mononuclear cellsPeripheral blood mononuclear cellsIL-27 expressionIL-10 levelsAnti-nuclear antibodiesEffector T cellsLevels of IFNCentral memory cellsLess IL-10Markers of efficacyBlood mononuclear cellsExpression of CD86Immune regulatory pathwaysIL-10 inductionHuman immune cellsHuman stool samplesImmunosuppressive medicationsIL-27Xenograft rejectionImmune therapyMononuclear cellsAntibiotic treatmentIL-27 LIMITS TYPE 2 IMMUNOPATHOLOGY FOLLOWING PARAINFLUENZA VIRUS INFECTION
Muallem G, Wagage S, Sun Y, DeLong JH, Valenzuela A, Christian DA, Pritchard G, Fang Q, Buza EL, Jain D, Elloso MM, López CB, Hunter CA. IL-27 LIMITS TYPE 2 IMMUNOPATHOLOGY FOLLOWING PARAINFLUENZA VIRUS INFECTION. PLOS Pathogens 2017, 13: e1006173. PMID: 28129374, PMCID: PMC5305264, DOI: 10.1371/journal.ppat.1006173.Peer-Reviewed Original ResearchConceptsParainfluenza virus infectionTh2 responsesIL-27Control miceT cellsVirus infectionParamyxovirus infectionDisease severityWeight lossPathogenic Th2 responsesQuality of CD4Type 2 immunopathologyT-cell depletionT cell responsesSevere lung lesionsPopulation of IFNParainfluenza infectionsPulmonary eosinophilsRespiratory paramyxovirusesT helperCell depletionLung lesionsImmune responseLimit pathologyCD4
2013
Studying the Role for CD4+ T Cell Subsets in Human Lupus
Kang I. Studying the Role for CD4+ T Cell Subsets in Human Lupus. 2013 DOI: 10.21236/ada585488.Peer-Reviewed Original ResearchIL-27IL-1Autoimmune complexesTh17 cellsLupus patientsPro-inflammatory cytokines IL-1Human monocytesExogenous IL-27IL-17 productionTh cell responsesT cell subsetsToll-like receptorsProduction of cytokinesIL-27 geneCytokines IL-1IL-1 expressionPotential therapeutic implicationsIL-10Human lupusCell subsetsPolarizing cytokinesT cellsHuman CD4Therapeutic implicationsPatients
2011
B Cells as a Therapeutic Target for IFN-β in Relapsing–Remitting Multiple Sclerosis
Ramgolam V, Sha Y, Marcus K, Choudhary N, Troiani L, Chopra M, Markovic-Plese S. B Cells as a Therapeutic Target for IFN-β in Relapsing–Remitting Multiple Sclerosis. The Journal Of Immunology 2011, 186: 4518-4526. PMID: 21368231, DOI: 10.4049/jimmunol.1000271.Peer-Reviewed Original ResearchConceptsRR-MS patientsIFN-β-1bRelapsing-remitting multiple sclerosisCell stimulatory capacityStimulatory capacityB cellsMS patientsUntreated patientsIL-23IL-27IL-12Multiple sclerosisIL-1βProliferative responseAg-specific T cell proliferative responsesFirst-line immunomodulatory therapyT cell proliferative responsesSuppression of CD40Low proliferative responseB-cell secretionCell proliferative responsesB cell functionMHC class IRR-MSImmunomodulatory therapy
2008
Epstein‐Barr virus‐induced gene 3 negatively regulates IL‐17, IL‐22 and RORγt
Yang J, Yang M, Htut TM, Ouyang X, Hanidu A, Li X, Sellati R, Jiang H, Zhang S, Li H, Zhao J, Ting AT, Mayer L, Unkeless JC, Labadia ME, Hodge M, Li J, Xiong H. Epstein‐Barr virus‐induced gene 3 negatively regulates IL‐17, IL‐22 and RORγt. European Journal Of Immunology 2008, 38: 1204-1214. PMID: 18412165, PMCID: PMC2989250, DOI: 10.1002/eji.200838145.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCell DifferentiationForkhead Transcription FactorsGene ExpressionGene Expression RegulationInterferon-gammaInterleukin-17InterleukinsListeria monocytogenesListeriosisMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMinor Histocompatibility AntigensNuclear Receptor Subfamily 1, Group F, Member 3OvalbuminReceptors, Antigen, T-CellReceptors, Retinoic AcidReceptors, Thyroid HormoneSpleenT-LymphocytesT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaConceptsIL-17IL-22Th17 cellsIL-27Spleen cellsRORgamma tEpstein-Barr virus-induced gene 3IL-17-producing cellsReduced bacterial loadIL-35Protective immunityIL-12p35Th17 conditionsAdaptive immunityEBI3Mouse studiesL. monocytogenesBacterial loadMiceElevated levelsAcute challengeGene 3High levelsP28ImmunityInterferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS)
Ramgolam V, Speer D, Markovic‐Plese S. Interferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS). The FASEB Journal 2008, 22: 1074.8-1074.8. DOI: 10.1096/fasebj.22.1_supplement.1074.8.Peer-Reviewed Original ResearchIFN beta-1aDendritic cellsIL-27Beta-1aMultiple sclerosisIL-23IL-1 betaIL-1betaPathogenesis of MSIL-23 promotesIL-27 expressionTh-17 cellsMature dendritic cellsInterferon beta-1aIL-1B expressionCytokines IL-6Cytokine gene expressionInduction of SOCS3Cell differentiationSTAT-1 activationExpression of SOCS3STAT-1 geneQuantitative RT-PCRMS patientsStandard therapy
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